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    Home > Active Ingredient News > Study of Nervous System > Heavy! After 6 years, the "Chinese Clinical Guidelines for the Treatment of Nerve Repair for Idiopathic Facial Nerve Palsy (2022 Edition)" was released!

    Heavy! After 6 years, the "Chinese Clinical Guidelines for the Treatment of Nerve Repair for Idiopathic Facial Nerve Palsy (2022 Edition)" was released!

    • Last Update: 2023-02-01
    • Source: Internet
    • Author: User
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    Idiopathic facial nerve palsy, also known as facial neuritis, Bell's palsy, traditional Chinese medicine called mouth seclusion, mouth and eye skew, is the most common facial nerve disease, accounting for 60% ~ 75%, the incidence is (11.
    5 ~ 53.
    3) / 100,000 people, clinical facial voluntary movement, expression function reduction or loss, facial nerve and facial expression muscle tissue nutritional disorders as the main manifestations, significantly affecting the patient's appearance, personal dignity and social image
    。 Severe patients have severe facial nerve edema, intrasheathal hypertension, facial nerve ischemia, hypoxia, and further aggravation of edema in the early stage of severe patients, resulting in axon necrosis, disintegration, and pathological changes
    of demyelinating in the early stage.
    In the later stage, it is dislocated and regenerated, causing facial cascade movement
    .


    At present, the treatment methods include drugs (dehydration drugs, B vitamins, glucocorticoids, antiviral drugs, etc.
    ), acupuncture, physiotherapy, facial rehabilitation training, etc
    .
    Most mild to moderate patients can basically recover after 2 weeks to 3 months of treatment, but there are more than 1/3 of the residual symptoms of moderate and severe patients, and the standardized treatment of integrated Chinese and Western medicine nerve repair can help improve the prognosis
    .


    Today, let's learn the latest guidelines on clinical manifestations, diagnosis, disease stage, differential diagnosis, clinical examination and treatment~



    Clinical manifestations


    The incidence is mainly concentrated in 20~40 years old, and more men are more
    .
    Most of the disease is unilateral, and the co-incidence of both sides is rare
    .
    A small number of patients can have recurrent attacks, the recurrence rate is 2.
    6%~15.
    2%, and
    the incidence is higher in spring and summer, reaching a peak
    in September.


    Often the onset is more urgent, usually manifested as crooked corners of the mouth on the affected side, leaky speech, unable to frown, close eyes, show teeth, puff out cheeks and other actions
    .
    When eating food, it often stays in the gap between the teeth and cheeks on the sick side, and saliva often flows down from the affected side
    .
    The tear punctum turns out with the lower eyelid, so that the tear cannot be drained according to normal and causes overflow
    .
    Some patients may have mild pain behind the ipsilateral ear and mastoid area a few days before the onset of illness, which can peak
    within 72 hours.
    During physical examination, it can be seen that the muscles of the affected side are paralyzed, the frontal lines on the affected side become shallow or disappear, the eye fissure increases, the nasolabial fold becomes shallow, and when the facial muscles move, the muscles in the healthy side contract normally, stretching the affected side These signs are more pronounced
    .
    The eyelid on the affected side cannot be closed, and when the eye is closed, the paralyzed eyeball turns outward and upward, revealing the white sclera, which is called the Bell phenomenon
    .


    Damage to different parts of the facial nerve presents with different clinical symptoms:


    (1) Preganglionic lesions: tymdal nerve damage, prelingual 2/3 taste disorders; damage to the nerve branches of the stapes muscle, the appearance of hypersensitivity to hearing;


    (2) Damage to the geniculate ganglia: not only facial nerve paralysis, hearing allergy and prelingual 2/3 taste disorders, but also auricle and external auditory canal dysesthesia, herpes on the external auditory canal and tympanic membrane, called Hunter syndrome, is associated with herpes zoster virus infection;


    (3) Lesions near the stem and breast hole: the above signs of peripheral facial paralysis and tenderness in the area behind the ear will occur
    .


    Patients with facial nerve palsy who do not recover completely are often accompanied by atrophy of paralyzed muscles, blephamospasm, joint movement, and pulling sensation in the affected side
    .
    The contracture of the paralyzed muscle is manifested as deepening of the nasolabial fold on the sick side, the corner of the mouth is tilted to the affected side, and the eye fissure is reduced; However, if the patient is allowed to do active exercises such as cheek bulging and teething, it can be found that the facial muscles on the affected side are abnormally contracted, while the muscles on the healthy side contract normally, and the eye fissure on the affected side is smaller
    .
    Blepharospasm is manifested by spasm
    of the muscles around the eye on the affected side when the face is slightly vigorous.
    Common clinical collateral signs include slight fluttering of the upper lip on the sick side of the patient's blink of sight; Involuntary closure of the sick eye during tooth display; contraction of the sick frontal muscles when trying to close the eyes; When eating and chewing, tearing on the sick side (crocodile tears) is accompanied by temporal skin flushing, local fever, and sweat secretion
    .



    Key points of diagnosis and stage of disease


    1.
    Key points of diagnosis


    (1) Acute onset, often have a history of cold and wind, or have a history of
    virus infection.


    (2) One side of the facial muscles is suddenly paralyzed, the frontal lines on the affected side disappear and become shallow, the eyelids cannot be closed, the nasolabial folds become shallow, the corners of the mouth are crooked, the cheeks are bulging and leaking, and the food is easy to stay between the teeth and cheeks of the sick side, which can be accompanied by loss of taste in the first 2/3 of the tongue on the sick side, hearing allergies, tears, etc
    .
    No other positive neurologic signs
    .


    (3) Brain CT and MRI examinations are normal
    .


    2.
    Stage of disease


    (1) Acute stage: within
    15 days of onset.


    (2) Recovery period: 16 days to 6 months
    of onset.


    (3) Sequelae period: more than
    6 months of onset.



    differential diagnosis


    Once a patient presents with facial palsy, it is first necessary to distinguish between central and peripheral facial palsy
    based on typical signs.


    Of peripheral facial palsy, 75% are idiopathic facial palsy and about 25% are due to other causes, which need to be differentiated in combination with other conditions:


    (1) Guillain-Barré syndrome: acute or subacute onset, often with a history of fever or diarrhea prodromal infection, sudden brackey paralysis of limbs, accompanied by bilateral peripheral facial palsy, protein-cell separation in cerebrospinal fluid
    .


    (2) Lyme neurotreponemal disease: mostly transmitted by tick bites, with a history of
    chronic erythema migrans or arthritis.


    (3) Diabetic nerve damage: often accompanied by other cranial nerve damage, mostly oculomotor nerve, abducens nerve and facial nerve damage, can occur single nerve
    .


    (4) Secondary facial nerve palsy: often secondary to parotid gland inflammation or tumors, otitis media and other diseases involving the facial nerve, but mostly accompanied by other clinical manifestations
    of the primary disease.
    Tumor compression can also lead to facial nerve paralysis, which is more common in pontine cerebellar angle tumors, such as acoustic neuroma and meningioma
    .


    (5) Traumatic facial paralysis: mostly caused
    by skull base fracture.



    Clinical grading and functional evaluation table

    1.
    Facial paralysis motor function evaluation scale


    Table 1 House-Brackmann grade of facial nerve palsy


    Table 2 Burres-Fisch facial nerve score


    Table 3 Sunnybrook (Toronto) facial nerve assessment system


    2.
    Facial paralysis quality of life evaluation scale

    Table 4 Facial Disability Index (FDI) scale



    Clinical examination


    1.
    Electrophysiology

    Neuroelectrophysiological detection technology is a means that can quickly detect facial nerve function, which can provide a reference for clinical prediction of prognosis and the selection of treatment methods, promote the maximum recovery of facial nerve function, and improve the quality of life of patients, which has important clinical guiding significance
    .
    Commonly used neuroelectrophysiological evaluation techniques include the following:

    (1) Neural excitability test (NET)

    Original.
    Theory:
    In the case of facial nerve injury, when the residual nerve fibers reach a certain number, it can cause the contraction of facial muscles under weak current stimulation, so as to evaluate the excitability of the facial nerve and provide an effective basis
    for later prognosis.

    Methods: The facial nerve stimulator was used to stimulate the nerve trunk below the mastole hole of the facial nerve stem, the frequency of the stimulation pulse was 1Hz, the time course was 1ms, and the minimum current intensity (stimulation threshold)
    that caused the contraction of facial muscles on both sides was determined.

    The results were judged: the stimulation threshold of the two sides was compared, if the two sides were 2~3.
    5mA apart, it indicated that there was neurodegeneration
    on the affected side.

    Prognosis suggests: 88% of those with positive neuroexcitability test within 10 days of onset can fully recover, 73% of those with weakened response can fully recover, and those who have no response within 10 days cannot recover
    .

    Caution for use: Not suitable
    for bilateral facial nerve palsy.

    (2) Maximum stimulation test (MST)

    Methods: The facial nerve stimulation instrument combined with super current was used to stimulate the facial nerve trunk, so that all facial nerve fibers were excited, and the muscle contraction intensity of the unaffected side and the affected side was compared and divided into four levels
    .
    If muscle contraction on the affected side is significantly weakened or movement is lost, it reflects poor recovery of facial nerve function and a poor
    prognosis.

    (3) Concentric needle electrode electromyography (EMG)

    Electromyography can quickly and objectively reflect the functional status of the neuromuscular itself, and is currently the best qualitative detection method of facial paralysis
    .

    Method: The action potential of the quadratus upper lip muscle was recorded with concentric circle needle electrodes, and the muscle was resting potential at normal rest, and the muscle would have a two-phase or three-phase potential when contracted at will
    .
    Prolonged insertion potential, fibrillation potential, positive sharp wave, moderate decrease in recontraction recruitment potential, etc.
    indicate abnormality
    .

    Detection time and prognosis: EMG detection should be carried out after 2~3 weeks of lesions, the detection time is too early, due to incomplete axonal degeneration, only partial abnormalities are shown, and the detection time is too late, and the disease course may not be detected by axonal injury
    .
    The failure to detect evoked potentials for 2~3 weeks suggests complete denervation damage, serious damage, and poor
    prognosis.
    If evoked potentials can be recorded, the latency period is normal, indicating neuroxic
    .

    (4) Induced electromyography and electromyography (EnoG)

    Electromyography, also known as evoked electromyography, is a method in which double-stimulated electrodes stimulate the facial nerve at the stem and mammary foramen and record the compound action potential of the perioral muscle groups innervated by each peripheral branch (CMAP)
    。 Using super stimulation, comparing the bidirectional compound action potential of the healthy side and the affected side, the percentage of amplitude reduction is used to indicate the degree of
    nerve changes.

    Results were judged that the degree of neurodegeneration within 3 weeks was less than 90% recommended conservative treatment
    .
    If the degree of onset 4d reaches 50%, degeneration in 6d reaches 90%, or the degree of 2d internal degeneration increases by more than 15%~20%, indicating that there are indications
    for surgical exploration.

    Advantages of electroneurography : it can quantitatively analyze the degree of
    nerve axon damage.

    2.
    Conventional magnetic resonance and high-resolution magnetic resonance head facial neurology multimodal imaging examination

    MRI of the facial nerve and internal auditory tract MRI are essential to exclude tumors such as acoustic neuromas, facial neuromas, cholesteatomas, and
    meningiomas.

    3.
    Ultrasonography

    Ultrasound can assess the size, echo, and blood flow
    of the facial nerve.
    High-frequency ultrasound as A complementary technique combined with neuroelectrophysiology that establishes normal values
    of the facial nerve.


    treat


    1.
    Principles of treatment


    (1) Integrated Chinese and Western medicine;


    (2) Acute stage: rest and recuperate, reduce adverse stimuli, focus on strengthening neuroprotection;


    (3) Recovery period and sequelae period: active nerve repair, moderate procedure activates hibernating nerves, and promotes good nerve regeneration;


    (4) Internal and external treatment, scientific rehabilitation training and treatment, saturated nerve repair
    .


    2.
    Oral medication


    (1) When there is evidence of viral infection such as shingles in the acute stage, antiviral drugs (such as acyclovir, valacyclovir) can be given orally; Neurotrophic categories include methylcobalamin and vitamin B1 oral; Prednisone tablets and other glucocorticoids are taken orally
    .
    Dialectical choice of oral Chinese medicine decoction
    .


    (2) It is recommended to continue to use neurotrophic drugs
    during the recovery period.


    (3) Patients with sequelae can use neurotrophic drugs
    intermittently as appropriate.


    3.
    Intramuscular and intravenous drugs


    (1) The use of dehydrating agent in the acute stage can reduce neuroedema, usually using mannitol 125~250ml intravenous drip, 2 times a day; Methylcobalamin 0.
    5mg, intramuscular injection, once every 1~2 days; dexamethasone 5mg into a pot 1~2 times a day (or choose escinin sodium, methylprednisolone, etc.
    ); Drugs such as fasudil improve microcirculation; Murine nerve growth factor 30 μg intramuscularly administered once daily
    .
    Ginkgo biloba extract 15ml, intravenous drip, once a day, 7~10d for 1 course of treatment
    .
    2~4 courses
    can be repeated.


    (2) Patients in the recovery period and sequelae can intermittently use neurotrophic drugs
    .


    4.
    Stellate ganglion block


    Suitable for patients
    at all stages of clinical practice.


    Operation: The patient goes to the pillow to lie flat, a thin pillow under the shoulder, and the head is tilted back, fully exposing the patient's neck
    .
    The surgeon's left hand is placed next to the trachea at the lower edge of the annular cartilage, which is equivalent to the level of the first annular cartilage, and after touching the carotid artery at the inner edge of the sternocleidomastoid muscle, it goes down the tracheal wall and the fingertip After palpation of the C6 transverse anterior tubercle, the surgeon holds a 7-gauge needle syringe in his right hand, from both The needle is inserted vertically between the fingers, and the tip of the needle can touch the anterior nodule of the C6 transverse process
    .
    The needle was fixed with the left hand and withdrawn, and no blood and cerebrospinal fluid were seen in the aspirate, suggesting that the drug
    could be injected.
    The presence of Horner syndrome on the affected side is a sign of successful blockade, which is manifested as reddening face, drooping eyelids, conjunctival hyperemia, pupil constriction and other clinical manifestations
    .


    Drug preparation: 2% lidocaine 5 mL + methylcobalamin 0.
    5 mg + vitamin B1 100 mg + dexamethasone (or triamcinolone acetonide) formulated as a 10 mL analgesic complex
    .


    Dosage: If dexamethasone is used in analgesic complex, dexamethasone 5mg on days 1~7, 2mg on days 8~15, once a day; If triamcinolone acetonide is used, triamcinolone acetonide 4 mg is treated once every 5 days
    .
    15 days is a course of treatment
    .


    Contraindications: prolongation of coagulation time or anticoagulation therapy; High fear of non-cooperatives; local inflammation, tumors, tracheostomy; Those
    who cough strongly and persistently.


    5.
    Hyperbaric oxygen


    It is mainly used in patients
    in the acute phase.


    The specific methods can be: treatment pressure 2 ATA, oxygen inhalation for 30min, rest for 5min and continue oxygen intake for 30min, 10d for 1 course
    .


    Medical Pulse Compiled from: Bu Yunyun, Chen Lin, Dai Yiwu.
    Clinical guidelines for the treatment of nerve repair in idiopathic facial palsy in China (2022 edition)[J/OL].
    Nerve injury and functional reconstruction:1-12[2023-01-05].


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